Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands.
Headache. 2012 Sep;52(8):1298-318. doi: 10.1111/j.1526-4610.2012.02162.x. Epub 2012 May 8.
Migraine patients are at an increased risk for stroke, as well as other thromboembolic events. This warrants further study of the role of platelets in a proportion of migraine patients.
To extend the "platelet hypothesis" using literature data and observations made in a rat model of shear stress-induced platelet aggregation. Such aggregation causes release of serotonin, leading to vasoconstriction during sufficiently strong aggregation and to long-lasting vasodilation when aggregation diminishes. This vasodilation also depends on nitric oxide and prostaglandin formation.
A role for platelet aggregation in a number of migraineurs is indicated by reports of an increased platelet activity during attacks and favorable effects of antiplatelet medication. We hypothesize that in those patients, a migraine attack with or without aura may both be caused by a rise in platelet-released plasma serotonin, albeit at different concentration. At high concentrations, serotonin may cause vasoconstriction and, consequently, the neuronal signs of aura, whereas at low concentrations, it may already stimulate perivascular pain fibers and cause vasodilation via local formation of nitric oxide, prostaglandins, and neuropeptides. Platelet aggregation may be unilaterally evoked by elevated shear stress in a stenotic cervico-cranial artery, by reversible vasoconstriction or by other cardiovascular abnormality, eg, a symptomatic patent foramen ovale. This most likely occurs when a migraine trigger has further enhanced platelet aggregability; literature shows that many triggers either stimulate platelets directly or reduce endogenous platelet antagonists like prostacyclin.
New strategies for migraine medication and risk reduction of stroke are suggested.
偏头痛患者发生中风和其他血栓栓塞事件的风险增加。这使得进一步研究血小板在部分偏头痛患者中的作用变得尤为重要。
利用文献数据和在大鼠剪切应力诱导血小板聚集模型中观察到的结果，扩展“血小板假说”。这种聚集会导致 5-羟色胺释放，从而导致聚集足够强时的血管收缩和聚集减弱时的持久血管扩张。这种血管扩张还依赖于一氧化氮和前列腺素的形成。
有报道称，偏头痛发作期间血小板活性增加，抗血小板药物治疗效果良好，这表明在一些偏头痛患者中，血小板聚集可能在偏头痛发作（有或无先兆）中起作用。我们假设，在这些患者中，偏头痛发作（有或无先兆）可能都是由血小板释放的血浆 5-羟色胺升高引起的，尽管浓度不同。在高浓度时，5-羟色胺可能导致血管收缩，从而引发先兆症状；而在低浓度时，它可能已经刺激了血管周围的疼痛纤维，并通过局部形成一氧化氮、前列腺素和神经肽引起血管扩张。血小板聚集可能是由狭窄的颈颅动脉中升高的剪切应力、可逆性血管收缩或其他心血管异常（例如有症状的卵圆孔未闭）单侧引发的。这最有可能发生在偏头痛触发因素进一步增强血小板聚集性的时候；文献表明，许多触发因素直接刺激血小板或减少内源性血小板拮抗剂，如前列腺素 I2。
建议采取新的偏头痛药物治疗策略和降低中风风险的策略。
